Conversion of paroxysmal supraventricular tachycardia due to a concealed extranodal pathway with intravenous bolus of lidocaine.
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Biomedical subjects
Publications and source records attributed to D Wu.
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Disopyramide phosphate was administered intravenously to 57 patients with 60 episodes of arrhythmia (21 supraventricular and 39 ventricular) as a 2 mg/kg bolus. Conversion to sinus rhythm was achieved in three (38 percent) of eight patients with atrial flutter, two (20 percent) of ten patients with atrial fibrillation, one (33 percent) of three patients with paroxysmal atrial tachycardia, and two (50 percent) of four patients with sustained ventricular tachycardia. In nine (75 percent) of 12 patients with nonsustained ventricular tachycardia, suppression of the arrhythmia was accomplished following the intravenous bolus of disopyramide. In 18 (78 percent) of 23 patients with frequent ventricular premature contractions, greater than 50 percent suppression of the ventricular premature contractions was achieved. These effects were satisfactorily maintained in six (86 percent) of seven patients with nonsustained ventricular tachycardia and in 14 (88 percent) of 16 patients with frequent ventricular premature contractions in whom therapy with disopyramide phosphate was continued as a 20 mg/hour intravenous drip infusion for up to 24 hours. Side effects were observed in only eight patients (14 percent) and were primarily anticholinergic in nature. Transient hypotension, not necessitating treatment with pressor agents, was observed in three patients (5 percent), in two of whom discontinuance of therapy with disopyramide was deemed necessary. Intravenous therapy with disopyramide in the dosage regimen employed appears to be moderately effective against supraventricular arrhythmia and particularly effective against ventricular arrhythmia with minimal toxicity. It appears to be a suitable alternative to intravenous therapy with lidocaine and has the additional advantage of availability for oral administration.
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Electrophysiologic studies were done in 32 patients with aortic stenosis. In 24 patients with intact A-V conduction, A-H intervals ranged from 55 to 145 msec and were prolonged in two. Two had split His bundle potentials. The H-V intervals ranged from 25 to 94 msec and were prolonged in 12. The mean H-V interval was 63 +/- 2.6 msec in 12 patients with calcific aortic stenosis compared with 50 +/- 4.9 msec in 12 without calcification (P less than 0.05). The mean H-V in 10 patients with aortic gradients greater than 40 mm Hg was 62 +/- 5.6 msec compared with 47 +/- 3.1 msec in nine with gradients less than 40 (P less than 0.05). In patients with aortic stenosis and A-V block, the site of the block was distal to the His bundle in three and within the His bundle in five. All eight had calcified valves. Aortic stenosis was commonly associated with latent and manifest conduction disease in the His bundle and the trifascicular conduction system. Conduction disease was more extensive with calcified valves and greater valve obstruction.
A family had an unusual and perhaps unique familial dysrhythmia. The proband had a short PR interval with normal QRS and chronic recurrent paroxysmal atrial tachycardia (Lown-Ganong-Levine syndrome). The arrhythmia produced left ventricular dysfunction. Both paroxysmal atrial tachycardia (PAT) and left ventricular dysfunction were reversed with administration of digoxin and propranolol hydrochloride. Three family members had paroxysmal or chronic atrial fibrillation, first diagnosed at a relatively young age (23 years, 38 years, and early 40s, respectively). Five additional family members had short PR intervals with normal QRS, and eight other family members had borderline short PR intervals. The mode of inheritance appeared to be autosomal dominant with varying expressivity. We have described a familial syndrome characterized by PAT or atrial fibrillation in its advanced form with short PR interval as a possible identifying trait. The future course of members with isolated short PR is unknown.
Although analysis of the surface electrocardiograms is usually sufficient in the diagnosis and management of patients with cardiac arrhythmias, electrophysiologic studies can improve diagnostic, therapeutic, and prognostic decisions. Indications for electrophysiologic studies appear to include the following: (1) asymptomatic patients with chronic second degree AV block, both type I and type II with or without bundle branch block; (2) asymptomatic patients with complete AV block; (3) symptomatic patients with bundle branch block and 1:1 AV conduction; (4) patients with bundle branch block complicating acute myocardial infarction; (5) patients with electrocardiograms suggesting pseudo AV block; (6) symptomatic patients with sinus bradycardia, in whom the causal relationship is not clear enough to justify pacing therapy; (7) patients with frequent, troublesome paroxysmal supraventricular tachycardia; (8) patients with Wolff-Parkinson-White syndrome and frequent paroxysmal supraventricular tachycardia; (9) patients with recurrent paroxysmal ventricular tachycardia; (10) patients with syncope or severe dizziness in whom the causal mechanism is not defined.
Prospective follow-up studies of 277 patients with chronic bifascicular block showed that 30 patients developed sudden cardiac death (SCD). Cumulative one-, two-, and three-year SCD mortality was computed. The patients that developed SCD were compared with the remaining patients (209 alive and 38 dead). The groups were similar in regard to age, sex, AH, and HV intervals. The following were more frequent in the SCD group (P less than .05): angina, previous myocardial infarction, heart failure, cardiomegaly, left bundle-branch block, premature ventricular beats, and ventricular tachycardia. Ventricular fibrillation was the cause of death in four cases of SCD where terminal ECG documentation was available. We concluded that SCD is a major cause of mortality in patients with chronic bifascicular block. The association of SCD with coronary disease and ventricular dysrhythmia suggested ventricular fibrillation as a frequent mechanism.
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His bundle electrograms were recorded in 308 adults with chronic bundle branch block. The A-H interval was normal in 249 patients and prolonged in 59. Comparison of patients with normal and prolonged A-H intervals revealed a greater incidence of demonstrable organic heart disease in the latter (P less than 0.01). Dyspnea, cardiomegaly and congestive heart failure were more frequent in patients with A-H prolongation. These patients also had longer P-R intervals and atrioventricular (A-V) nodal effective refractory periods, lower paced rates producing second degree A-V block proximal to the His bundle and a greater frequency of H-V prolongation. All patients were prospectively followed up in a conduction disease clinic with mean follow-up periods (+/- standard error of the mean) of 523 +/- 23 and 588 +/- 47 days in the patients with normal and prolonged A-H intervals, respectively. Seven (3 percent) of the patients with a normal A-H interval had A-V block with probable or definite site of block proximal to the His bundle in three and distal to the His bundle in four. In five of the six patients with a prolonged A-H interval who experienced A-V block (10 percent), the probable or definite site of block was proximal to the His bundle. Mortality (both sudden and nonsudden) was not significantly different in the patients with normal and prolonged A-H intervals. In summary, A-H prolongation was associated with increased incidence of organic heart disease and myocardial dysfunction. The risk of development of A-V nodal block was greater in patients with a prolonged A-H interval but appeared to be of minimal clinical significance.
Electrophysiologic studies were conducted in 17 patients without apparent sinus node disease before and after intravenous administration of 1 to 2 mg of atropine. Mean values in milliseconds (+/- standard error of the mean) before and after administration of atropine were as follows: sinus cycle length 846 +/- 26.4 versus 647 +/- 20.0 (P less than 0.001); sinus nodal recovery time 1,029 +/- 37 versus 774 +/- 36 (P less than 0.001); mean calculated sinoatrial (S-A) conduction time 103 +/- 5.7 versus 58 +/- 3.9 (P less than 0.001); mean P-A interval 34 +/- 1.5 msec versus 31 +/- 1.5 (P less than 0.05); mean atrial effective and functional refractory periods during sinus rhythm 285 +/- 11.3 versus 238 +/- 7.9 and 331 +/0 11.6 versus 280 +/- 8.6, respectively (P less than 0.001 for both); mean atrial effective and functional refractory periods measured at equivalent driven cycle length 239 +/- 7.7 versus 213 +/- 7.4 and 277 +/- 11.4 versus 245 +/- 9.5, respectively (P less than 0.001 for both). In conclusion, atropine shortened sinus cycle length, sinus nodal recovery time and calculated S-A conduction time. The shortening of atrial refractory periods with atropine implies that vagotonia prolongs atrial refractoriness in man.
Examination of the conduction system in three patients with bifascicular block who had electrophysiologic studies forms the basis for this report. Patients 1 and 2 had left bundle branch block and Patient 3 right bundle branch block and left axis deviation. The H-V interval was prolonged in each case (70, 65 and 60 msec, respectively). Serial section examination of the conduction system revealed sclerodegenerative involvement of both bundle branches in all cases. In Case 1, atrial extrastimulus testing converted left to right bundle branch block; in Case 2, it delineated a sinus echo zone with repetitive sinus nodal reentrance. In the latter case serial section revealed extensive amyloid infiltration of the approaches to the sinoatrial (S-A) node and the atrial preferential pathways. In Case 3, with right bundle branch block and left axis deviation, serial section revealed greater involvement of the anterior part of the main left bundle branch than of the posterior portion as well as involvement of the second part of the right bundle branch. The study revealed excellent correlation between electrophysiologic and pathologic findings in three cases of intraventricular conduction disease and demonstrated an anatomic basis for the electrophysiologic findings resembling alternating bilateral bundle branch block. Sinus nodal reentrance may be related to disease in the approaches to the S-A node thereby causing delay in perinodal tissue allowing sinus reentrance. Finally in Case 3, the anatomic substrate for left axis deviation may lie in a greater involvement of the anterior portion than of the posterior portion of the main left bundle rather than in the corresponding portions of the periphery.
Pre- and postoperative electrophysiologic studies are described that were suggestive of two (right- and left-sided) anomalous atrioventricular (A-V) connections in a patient with type B Wolff-Parkinson-White syndrome and intractable arrhythmias, who underwent epicardial mapping and successful surgical ablation of the right-sided anomalous pathway. The presence of the right-sided anomalous pathway capable of both antegrade and retrograde conduction was suggested by the following observations: (1) Type B preexcitation on the surface electro-cardiogram; (2) maximal preexcitation and minimal stimulus-delta with low lateral right atrial pacing; (3) epicardial mapping of the atria and ventricles; and (4) disappearance of ventricular preexcitation after surgical ablation of the right-sided anomalous pathway. The presence of an additional left-sided anomalous pathway capable of only retrograde conduction (concealed on the surface electrocardiogram) was sugg-sted by the following observations: (1) Left to right retrograde atrial activation sequence during reentrant tachycardia and ventricular pacing at rapid rates and with coupled ventricular pacing postoperatively; (2) spontaneous conversion of wide ORS tachycardia utilizing the anomalous pathway for antegrade conduction to narrow QRS tachycardia with significant slowing in rate; and (3) smooth antegrade A-V nodal conduction curves with echo zone postoperatively. The demonstration of bilateral anomalous pathway in patients with preexcitation has important electrophysiologic and surgical implications.
Electrophysiologic studies were conducted in 21 patients with sinus nodal dysfunction before and after intravenous administration of 1 to 2 mg of atropine. The mean sinus cycle length (+/- standard error of the mean) was 1,171 +/- 35 msec before and 806 +/- 29 msec after administration of atropine (P less than 0.001). Mean sinus nodal recovery time determined at a aced rate of 130/min and maximal recovery time were, respectively, 1,426 +/- 75 and 1,690 +/- 100 msec before and 1,169 +/- 90 and 1,311 +/- 111 msec after atropine (P less than 0.001 and less than 0.001). Mean calculated sinoatrial conduction time, measured in 16 patients, was 113 +/- 8 msec before and 105 +/- 9.7 msec after atropine (difference not significant). Mean atrial effective refractory period, measured at an equivalent driven cycle length, was 262 +/- 11.1 msec before and 256 +/- 10.3 msec after atropine (not significant). Mean atrial functional refractory period was 302 +/- 12.5 msec before and 295 +/- 11.3 msec after atropine (not significant). The shortening of sinus cycle length and sinus recovery time with atropine was similar to that noted in patients without sinus nodal dysfunction. In contrast, atropine had insignificant effects on sinoatrial conduction and atrial refractoriness in this group whereas it shortens both in normal subjects. This finding may reflect altered perinodal and atrial electrophysiologic properties in patients with sinus node disease.
A systematic study of retrograde atrial sequence at commonly used electrode catheter recording sites in 8 patients without, and in 4 patients with AV nodal re-entrant paroxysmal tachycardia was made. During right ventricular pacing, the retrograde atrial activation sequence was low septal right atrium--proximal coronary sinus--distal coronary sinus--high right atrium. During the episodes of paroxysmal tachycardia, a similar pattern was observed. This information should be helpful in the understanding of abnormal activation sequences in patients with paroxysmal supraventricular tachycardia in whom retrogradely conducting anomalous pathways are suspected.
The AV nodal conduction curve generated by the atrial extrastimulus technique has been described only qualitatively in man, making clinical comparison of known normal curves with those of suspected AV nodal dysfunction difficult. Also, the effects of physiological and pharmacological interventions have not been quantifiable. In 50 patients with normal AV conduction as defined by normal AH (less than 130 ms), normal AV nodal effective and functional refractory periods (less than 380 and less than 500 ms), and absence of demonstrable dual AV nodal pathways, we found that conduction curves (at sinus rhythm or longest paced cycle length) can be described by an exponential equation of the form delta = Ae-Bx. In this equation, delta is the increase in AV nodal conduction time of an extrastimulus compared to that of a regular beat and x is extrastimulus interval. The natural logarithm of this equation is linear in the semilogarithmic plane, thus permitting the constants A and B to be easily determined by a least-squares regression analysis with a hand calculator.
Electrophysiological studies (His bundle recordings and atrial stimulation) were performed in nine patients who manifested periods of both right and left bundle branch block (RBBB and LBBB). In seven of the patients, alternating bundle branch block appeared to reflect intermittent or chronic bundle branch block superimposed on incomplete (but electrocardiographically complete) block of the contralateral bundle branch. In three of these seven, shift from one bundle branch block pattern to the other was associated with reproducible change in H-V (mean change 30 msec), and could be induced by alteration of cardiac rate with carotid massage, coupled atrial stimulation, and rapid atrial pacing. In one of the seven, RBBB with a P-R of 0.20 seconds preceded chronic LBBB with a P-R of 0.24 seconds, implying that RBBB had been incomplete. In three of the seven, although a definite mechanism of alternation could not be demonstrated, transient contralateral bundle branch block occurred superimposed on chronic ipsilateral bundle branch block, implying that the ipsilateral block was incomplete. Two patients manifested periods of narrow QRS, LBBB, RBBB, and paroxysmal A-V block. Based upon pathological data (one case), this pattern appeared to reflect a lesion involving the distal His bundle and proximal bundle branches. In the total group of patients, clinical course was primarily determined by the severity of heart disease and not by occurrence of A-V block. The conduction defect in the majority of patients was surprisingly benign.
Eighteen of 388 patients with chronic bundle branch block, studied electrophysiologically and followed prospectively, had H-V intervals of 80 msec or greater. Five patients were functional class I, five class II, seven class III, and one class IV. Follow-up ranged from 103 to 1919 days (mean 711 +/- 118). Three patients needed permanent pacing for the following indications: sino-atrial block, sinus bradycardia post-cardiac surgery, and 2 degrees block distal to the His bundle. Six patients died, three suddenly, and three nonsudden. The five initially asymptomatic patients are alive and without pacemakers (mean follow-up 732 +/- 139 days). Although marked H-V prolongation was associated with high morbidity and mortality in this small series, this was only in patients with symptomatic heart disease. Asymptomatic patients (five patients) had a benign clinical course. Prophylactic pacing would probably not modify clinical course in the former group, and is probably not indicated in the latter group. Longer follow-up will be needed for definitive prognostication.
Seventeen consecutive patients with chronic recurrent ventricular tachycardia (VT) were studied in an attempt to delineate the reproducibility and mechanism of this arrhythmia. Six patients had nonsustained and 11 had sustained VT. The following electrophysiological techniques were utilized in an attempt to reproduce VT: 1) rapid atrial and ventricular pacing (17 pts); 2) atrial extrastimulus technique (17 pts); 3) ventricular extrastimulus technique (17 pts); 4) V1V2V3 stimulation technique (5 pts); 5) ventricular pacing from two or more sites (5 pts). Ventricular tachycardia was induced in six of 11 (54%) patients with sustained VT. However, in four there was only a single induction and only in the remaining two patients could VT be repetitively induced. In the latter two patients ventricular tachycardia was induced with both atrial and ventricular stimulation. Ventricular tachycardia could not be induced in any patient with nonsustained VT, although three had spontaneous episodes of ventricular tachycardia during study. In conclusion, in the present series of patients with chronic recurrent VT, this rhythm could not be reproducibly induced in the majority of patients in the cardiac catheterization laboratory utilizing catheter stimulation techniques.